目的基于公共数据库分析驱动蛋白家族成员26B(kinesin family member 26B,KIF26B)在膀胱癌中的表达水平,并探讨沉默KIF26B对膀胱癌细胞增殖、侵袭、迁移的影响。方法基于GEO和UaLcan数据库分析KIF26B在膀胱癌中的表达及与患者生存预后...目的基于公共数据库分析驱动蛋白家族成员26B(kinesin family member 26B,KIF26B)在膀胱癌中的表达水平,并探讨沉默KIF26B对膀胱癌细胞增殖、侵袭、迁移的影响。方法基于GEO和UaLcan数据库分析KIF26B在膀胱癌中的表达及与患者生存预后的关系;实时荧光定量聚合酶链反应(real-time quantitative polymerase chain reaction,RT-qPCR)和Western blot法检测膀胱癌细胞系(T24、J82)及膀胱正常上皮细胞SV-HUV-1中KIF26B的表达水平;将si-KIF26B、si-NC片段转染至T24细胞,采用噻唑蓝(methyl thiazolyl tetrazolium,MTT)法、Transwell实验和划痕实验检测沉默KIF26B后对T24细胞增殖、侵袭和迁移的影响;Western blot法检测沉默KIF26B后丝裂原活化蛋白激酶激酶(mitogen-activated protein kinase kinase,MEK)、磷酸化丝裂原活化蛋白激酶激酶(phosphorylated mitogen-activated protein kinase kinase p-MEK)、细胞外调节蛋白激酶(extracellular signal-regulated kinases,ERK)、磷酸化细胞外调节蛋白激酶(phosphorylated extracellular regulatory protein kinase,p-ERK)蛋白的表达水平。结果KIF26B在膀胱癌组织中高表达,KIF26B高表达患者的预后更差(P<0.05)。KIF26B在膀胱癌细胞系T24、J82中的表达水平显著高于膀胱正常上皮细胞SV-HUV-1(P<0.05)。沉默KIF26B基因后,MTT、Transwell和划痕实验结果显示,T24细胞的增殖、侵袭、迁移能力明显下降(P<0.05);沉默KIF26B后,T24细胞中p-MEK、p-ERK蛋白的表达下调(P<0.05),而MEK、ERK蛋白无明显变化(P>0.05)。结论KIF26B在膀胱癌组织和细胞中高表达,与患者预后不良相关,沉默KIF26B可抑制膀胱癌细胞增殖、侵袭和迁移,其机制可能通过MEK/ERK通路发挥作用。展开更多
Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+in...Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+independent anion reverse transporter and has not been reported in myocardial IR injury.Objectives:Tofind potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury.Methods:RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment.Myocardial infarction size was detected by TTC staining.Serum CK,creatinine kinase-myocardial band,Cardiac troponin I,and lactate dehydrogenase levels were determined by ELISA.The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting.The effects of SLC26A4 on inflammation were determined by HE staining,ELISA,and real-time PCR.The effect of SLC26A4 on the NF-κB pathway was determined by western blotting.Results:SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment.Compared with IR rats,those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size,reduced serum LDH/CK/CK-MB/cTnI levels,and elevated left ventricular ejection fraction and fractional shortening.SLC26A4 silencing inhibited myocardial inflammation,cell apoptosis,phosphorylation,and nuclear translocation of NF-κB p65.Conclusion:SLC26A4 exhibited promoting effects on myocardial IR injury,while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway.These results further unveil the role of SLC26A4 in IR injury.展开更多
癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(supe...癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(super refractory status epilepticus,SRSE),SRSE是一种罕见的破坏性疾病,儿童SRSE的病死率可达13.3%[2],若未经及时救治,可导致机体内环境紊乱、多脏器功能障碍等,甚至危及生命,存活者往往存在不同程度的脑损伤。展开更多
基金This study was funded by the Joint Guidance Project of Heilongjiang Provincial Natural Science Foundation of China(LH2023H063)the Scientific Research Project of Academic Thought Inheritance of Chinese Medicine Great Master of Heilongjiang Provincial Administration of Traditional Chinese Medicine(ZHY2023-151).
文摘Introduction:Myocardial ischemia-reperfusion(IR)injury has received widespread attention due to its damaging effects.Electroacupuncture(EA)pretreatment has preventive effects on myocardial IR injury.SLC26A4 is a Na+independent anion reverse transporter and has not been reported in myocardial IR injury.Objectives:Tofind potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury.Methods:RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment.Myocardial infarction size was detected by TTC staining.Serum CK,creatinine kinase-myocardial band,Cardiac troponin I,and lactate dehydrogenase levels were determined by ELISA.The effect of SLC26A4 on cardiomyocyte apoptosis was explored by TUNEL staining and western blotting.The effects of SLC26A4 on inflammation were determined by HE staining,ELISA,and real-time PCR.The effect of SLC26A4 on the NF-κB pathway was determined by western blotting.Results:SLC26A4 was up-regulated in IR rats but downregulated in IR rats with EA pretreatment.Compared with IR rats,those with SLC26A4 knockdown exhibited improved cardiac function according to decreased myocardial infarction size,reduced serum LDH/CK/CK-MB/cTnI levels,and elevated left ventricular ejection fraction and fractional shortening.SLC26A4 silencing inhibited myocardial inflammation,cell apoptosis,phosphorylation,and nuclear translocation of NF-κB p65.Conclusion:SLC26A4 exhibited promoting effects on myocardial IR injury,while the SLC26A4 knockdown had an inhibitory effect on the NF-κB pathway.These results further unveil the role of SLC26A4 in IR injury.
文摘癫痫持续状态(status epilepticus,SE)是儿童急重症,年均发病率17~23/10万[1],控制不佳易转变为难治性癫痫持续状态(refractory status epilepticus,RSE),其中通过全身麻醉治疗24h后发作仍未终止的RSE被称为超级难治性癫痫持续状态(super refractory status epilepticus,SRSE),SRSE是一种罕见的破坏性疾病,儿童SRSE的病死率可达13.3%[2],若未经及时救治,可导致机体内环境紊乱、多脏器功能障碍等,甚至危及生命,存活者往往存在不同程度的脑损伤。
